Our results also suggested that IL-6 Amplifier loop activation induces the NFκB and STAT3 signalling pathway activation in the non-immune cells like fibroblast derived from CABMR patients. Gene expression analysis of IL-6, MCP1, and CCL20 was significantly higher with synergistic activation of IL-6 and IL-17 as compared to either IL-6 or IL-17 alone, while SOCS3 gene expression was downregulated. RESULTS: IL-6 and IL-17 synergistically induced more IL-6, CCL-20 & MCP-1 production from fibroblasts. mRNA expression of IL-6, MCP1, CCL20, and SOCS3 genes were measured in the stimulated fibroblasts. Levels of IL-6, MCP-1, and CCL20 were estimated in culture supernatants by ELISA as marker of IL-6 amplifier loop activation. METHODS: Fibroblasts from grafted kidney from CABMR patients (n = 6) were cultured and stimulated with IL-6 (20 ng/ μl), IL-17 (50 ng/ μl), IL-6 plus IL-17 for 24 hours. Recently, non-immune cells like fibroblast have been postulated to mediate chronic allograft rejection via activation of IL-6 amplifier loop (IL-6+IL-17) via NFκB and STAT3 signaling pathway.ĪIM OF THE STUDY: We evaluated IL-6 amplifier loop activation by IL-6 and Il-17 in chronic antibody-mediated rejection (CABMR) in renal transplant recipient. BACKGROUND: IL-6 is a most important cytokine that plays a central role in the development of chronic inflammation.
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